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作 者:Jun-Hua Liang Jian-Ping Jia
机构地区:[1]Department of Neurology, Xuan Wu Hospital of the Capital Medical University
出 处:《Neuroscience Bulletin》2014年第2期308-316,共9页神经科学通报(英文版)
摘 要:Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer's disease (AD). The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.Neuronal autophagy is essential for neuronal survival and the maintenance of neuronal homeostasis. Increasing evidence has implicated autophagic dysfunction in the pathogenesis of Alzheimer's disease (AD). The mechanisms underlying autophagic failure in AD involve several steps, from autophagosome formation to degradation. The effect of modulating autophagy is context-dependent. Stimulation of autophagy is not always beneficial. During the implementation of therapies that modulate autophagy, the nature of the autophagic defect, the timing of intervention, and the optimal level and duration of modulation should be fully considered.
关 键 词:Alzheimer's disease AUTOPHAGY PRESENILIN AXON LYSOSOME animal model
分 类 号:R749.16[医药卫生—神经病学与精神病学]
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